Lactation in the rat is characterized by an inhibition of ovarian cyclicity which correlates with a suppression of gonadotropin secretion. The proposed studies are designed to examine how the suckling stimulus and the elevated levels of prolactin associated with lactation suppress pituitary and hypothalamic function. The suppression of pituitary function is manifested as a decrease in all modes of LH secretion whereas only the postcastration rise in FSH secretion is suppressed. Based on in vitro studies, the LH response to GnRH and the rate of LH synthesis and release are decreased during lactation. Studies are designed to determine which factors associated with lactation are responsible for the differential effects on LH and FSH secretion. Experiments will be performed to establish the mechanisms by which lactation decreases the rate of LH release in the face of elevated stores in pituitary. The hypothesis will be tested that the deficits in pituitary function during lactation are the result of a decrease in endogenous GnRH secretion. Animals will be exposed to various pulsatile GnRH replacement regimens to determine whether gonadotropin secretion can be restored to normal in the continued presence of the suckling stimulus. Studies to delineate the effects of lactation on hypothalamic function will focus on the control GnRH secretion. Concentrations of GnRH in hypophyseal portal blood will be measured during lactation and the strous cycle. GnRH measurements will also be made after electrical stimulation of the arcuate nucleus, and the effects of changes in the intensity of the suckling stimulus and in prolactin concentrations will be assessed. The effects that the changes in dopamine activity associated with lactation have on gonadotropin secretion will be assessed as will be possibility that increased opiate activity may be involved in mediating the effects of the suckling stimulus. These studies should provide insight into the mechanisms by which lactation suppresses reproductive cyclicity.